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K D Pool

Publications and source records attributed to K D Pool.

14 recordsLinked to original sources
PubMed1994

Linguistic performance and regional cerebral blood flow in persons who stutter.

In a series of studies regarding CNS dysfunction in stuttering, we have examined linguistic and motoric performance in the context of measures of brain function. Previous studies of adults with developmental stuttering identified alterations in brain function (metabolic and electrophysiologic) in cortical regions implicated in models of speech motor control and language processing. We also identified a sub-group of these subjects who exhibited linguistic performance deficits related to speech performance deficits. The present study examined the hypothesis that adults who stutter and who show linguistic performance deficits will also show metabolic alterations in cortical regions classically related to language processing, whereas adults who stutter but who do not show linguistic performance deficits will not show these cortical metabolic alterations. Significant relative blood flow asymmetry (left < right) was observed in middle temporal and inferior frontal cortical regions only for adults who both stuttered and showed linguistic performance deficits. Results support models that explicitly recognize that efficient integration of linguistic, motoric, and cognitive processes is critical to the production of oral/verbal fluency and to understanding sources of fluency failure.

Adult↗
PubMed1992

Brain blood flow related to acoustic laryngeal reaction time in adult developmental stutterers.

The 1980s witnessed renewed interest in the relation between developmental stuttering and central nervous system (CNS) abnormalities. We have reported differences between nonstutterers and developmental stutterers on electrophysiologic (QTE) and metabolic (rCBF) measures of brain function. A critical step in the interpretation of results of functional brain imaging studies is to determine the relation, if any, of identified CNS abnormalities to speech motor control in persons who stutter. In this study we addressed the interpretation of rCBF findings by asking whether we could identify patterns of impaired acoustic laryngeal reaction time (LRT) as a function of response complexity parallel to rCBF findings. Stutterer subgroups determined by clinical severity ratings were not differentiated by LRT values as a function of response complexity. Stutterers with relative blood flow asymmetry below the normal median value involving both left superior and middle temporal regions of interest (ROIs) showed significantly longer LRT for the complex response than did normal speakers and stutterers with above-normal median relative flow values to at least one of these temporal ROIs. Stutterer subgroups based on reduced cingulate flow alone were not differentiated by LRT values. Findings are consistent with Goldberg's (1985) model of CNS premotor processing. Findings also suggest that stutterer subgroups might be distinguished by the presence, loci, and relative magnitude of cortical and/or subcortical rCBF abnormality in regions that subserve a fluency-generating system.

Adult↗
PubMed1991

Heterogeneity in spasmodic dysphonia. Neurologic and voice findings.

Spasmodic dysphonia is a disturbance of phonation with laryngeal spasms. We report voice and neurologic examination findings in 45 subjects. Neurologic abnormalities were found in 32 subjects (71.1%). Rapid alternating movement abnormalities, weakness, and tremor were common. Incoordination and spasticity were rare. Lower extremity findings were frequent. Abnormalities were bilateral. Spasmodic dysphonia severity was related to age. Type, severity, and duration of vocal symptoms were not different for subjects with or without neurologic abnormalities. Vocal tremor was more frequent in neurologically abnormal subjects. Involvement of a pallidothalamic-supplementary motor area system could account for neurologic findings, brain imaging findings, and clinical heterogeneity. The view emerging is that spasmodic dysphonia is a manifestation of disordered motor control involving systems of neurons rather than single anatomical sites.

Adult↗
PubMed1991

Regional cerebral blood flow in developmental stutterers.

Stuttering is a poorly understood communication disorder with a 1% global prevalence. Recently, there has been a resurgence of interest in a neurogenic origin for the disorder, although no research has established clear neurological differences between "developmental" (stuttering onset in childhood) stutterers and nonstutterers. We have used xenon 133 single-photon emission computed tomography to study regional cerebral blood flow (rCBF) in 20 stutterers. Analysis revealed global, absolute flow reductions. Relative flow asymmetries (left less than right) were identified in three hemispheric regions: anterior cingulate and superior and middle temporal gyri. Milder changes were found in the left inferior frontal gyrus. Stutterers had rCBF values below median for either anterior cingulate or middle temporal gyri. With one exception, severe stutterers had rCBF values below median for the anterior cingulate gyrus. All stutterers with rCBF values above median in the cingulate gyrus had rCBF values below median in the middle temporal gyrus, and severity of their disorder was either mild or moderate. Our findings suggest that stuttering is a neurogenic disorder involving recognized cortical regions of speech-motor control.

Adult↗
PubMed1991

Laryngeal reaction time profiles in spasmodic dysphonia: relationship to cortical electrophysiologic abnormality.

This study combines measures of linguistic and vocal performance and long-latency auditory electrophysiology to investigate task-dependent variability in spasmodic dysphonia (SD). Linguistic performance was evaluated using several measures of relatively complex linguistic ability (i.e., discourse analysis). Vocal performance was evaluated by measuring acoustic laryngeal reaction time (LRT) for tasks that differ in complexity. Normal structure of the cortex and subcortex was confirmed by magnetic resonance imaging. Cortical function was measured using multichannel quantitative auditory evoked potentials (AEPs). As a group, SD subjects who demonstrated subtle linguistic deficits also demonstrated prolonged LRT for the complex task and repeated and persistent auditory electrophysiologic abnormalities over the anterior quadrant of the left hemisphere. As a group, linguistically normal SD subjects demonstrated no significant increase in LRT for the complex task and no recurrent electrophysiologic abnormalities over the left anterior cortex relative to normal controls. Results support a neurogenic origin of SD and suggest that some aspects of inter- and intrasubject variability may be related to differences in loci and magnitude of cortical abnormalities.

Adult↗
PubMed1991

Quantitative electroencephalography and anatomoclinical principles of aphasia. A validation study.

No single technology in isolation can provide a full view of the anatomoclinical principles evident in the clinical populations we study. The dynamic nature of quantitative electrophysiology makes it an ideal complement to anatomic and metabolic imaging. The statistical conundrum it has presented may be resolved by the approach incorporated in CART. The intent of this study was to examine QEEG and CART in the evaluation of the neurologic bases of a well-defined behavioral disorder like aphasia. The combined power of QEEG and CART yielded objective electrophysiologic methods to predict aphasia that rival the reliability of the language examination. Such success is unprecedented. This success allows us to incorporate QEEG and CART into our technological armamentarium and to return to the evaluation of less well-understood disorders with confidence in both our findings and anatomoclinical principles we derive from them.

Adolescent↗
PubMed1990

Quantitative topographic electrophysiology and functional neurologic status in right middle cerebral artery infarction.

Thirteen patients with clinically and radiographically defined right middle cerebral artery infarction were studied using EEG, quantitative electroencephalographic (QEEG) spectra, and multi-channel evoked potentials. The purpose of this effort was to develop QEEG rules that related to the patient's neurologic status. Three QEEG relative delta spectral patterns were identified in the right hemisphere which related to neurologic residua. These include limited perisylvian involvement, mixed involvement of perisylvian and extrasylvian regions, and extrasylvian involvement only. While there were parallels between QEEG spectral patterns and auditory, visual and somatosensory evoked potentials, there were modality specific features consistent with functional differences.

Aged↗
PubMed1990

Evidence for cortical dysfunction in spasmodic dysphonia: regional cerebral blood flow and quantitative electrophysiology.

Cortical function was evaluated in 26 subjects with spasmodic dysphonia. Quantitative topographic electrophysiologic mapping (QTE) was employed to provide quantitative analyses of EEG spectra and auditory and visual long-latency evoked potentials. Single-photon emission computed tomography (SPECT) of the cerebral transit of Xenon-133 was used to evaluate regional cerebral blood flow. Left hemispheric abnormalities in cortical function were found by both techniques in 10 subjects and by at least one technique in 18 subjects. Right hemispheric abnormalities were observed by both techniques in 8 subjects and by at least one technique in 18 subjects. Most patients with cortical dysfunction in one hemisphere had cortical dysfunction in the other, while only 4 subjects had unilateral lesions as found by one of the two techniques. Eight subjects were normal by all measurements. Underlying structural abnormalities were detected by magnetic resonance imaging in 5/24 subjects. However, functional abnormalities (SPECT or QTE) were not observed at sites of structural abnormalities. SPECT and QTE were significantly related in identification of left hemispheric dysfunction (p = .037) with a trend in the right hemisphere (p = .070), and a significant congruence of SPECT and QTE findings occurred in the left anterior cortical quadrant (p = .011). These findings indicate that dysfunction of cortical perfusion and/or cortical electrophysiology is associated with spasmodic dysphonia in the majority of subjects studied.

Adult↗
PubMed1989

Localization of multiple dipoles: mathematical programming approaches.

Although there has been progress in EEG and evoked potential analysis, the identification of underlying neural activity has eluded researchers despite its importance. This paper introduces the application of mathematical programming techniques to the "inverse" problem of three-dimensional localization of brain activity from scalp potentials. Preliminary computer experience with these optimization methods reported herein, yields encouraging results on simulated data and points new directions for research.

Brain Mapping↗
PubMed1989

Evaluation of a computer-automated program for clinical assessment of the auditory brain stem response.

An evaluation of an automatic auditory brain stem evaluation (AABE) for waves I, III, and V, of the auditory brain stem response (ABR) is presented. The on-line procedure performs a mathematical analysis of ABR waveforms using principles similar to those used by experienced clinicians to make threshold and latency decisions. It has been tested and applied to normal and pathologic traces at stimulus levels from 20 to 100 dB HL. Subject ages ranged from 6 months through adulthood. Latencies and thresholds determined by the analytic technique were examined and found to be indistinguishable from decisions of two "expert" observers and four practicing clinical audiologists experienced in ABR. Speed, practicality, and limitations of the software for routine ABR assessments are discussed.

Adolescent↗
PubMed1989

Infarction of the superior temporal gyrus: a description of auditory evoked potential latency and amplitude topology.

P1 and N1 of the cortical auditory evoked potential (AEP) were studied with multiple electrodes in 10 normal subjects and 6 patients with left middle cerebral artery infarction. Patients were selected based on neurological examination and on CT scans showing both (1) infarction limited to the vascular territory and (2) involvement of posterior portion of superior temporal gyrus. Waveforms recorded from C3, Cz, and C4 were examined for peak latency and amplitude of P1 and N1 on all subjects. Topographic displays of amplitude over P1 and N1 latency ranges were also examined. In normals, P1 was identified in 9 of the 10 subjects at all three electrode sites. In patients, P1 was identified at C3 in only 1 of the 6. N1 was present at all three electrodes in the 10 normal subjects and in 5 of the 6 patients. The remaining patient had N1 at C4 and Cz only. Examination of amplitude topology showed as asymmetric evolution of P1 and N1 in the patients. This asymmetry was not present in normals. The results of this study are consistent with theory that P1 arises from primary auditory cortex. Results further suggest multiple generators for N1. Additional study correlating topographic display from multichannel recordings with CT or MRI in brain-injured patients may bring more insight into N1 generators.

Adult↗
PubMed1987

Spasmodic dysphonia subsequent to head trauma.

Spasmodic dysphonia (SD) is a low-incidence voice disorder of unknown origin. A subgroup of seven patients with SD from our larger pool of 70 report vocal symptoms subsequent to head injury. This article is a case report of the neurodiagnostic findings, including computed tomography, magnetic resonance imaging, auditory brain-stem response, brain electrical activity mapping, and single photon emission computed tomography for three such patients. For each patient, two or more tests revealed positive neurologic findings. Each test, except computed tomography, demonstrated abnormalities in one or more patients. Two principles of clinical management are derived: (1) information regarding head trauma sustained before SD symptom onset is significant; (2) the absence of neuropathology on a single measure of central nervous system function should not be considered conclusive evidence that no neurologic lesions exist.

Adult↗